SUN-424 An Unusual Presentation of Delayed Onset Panhypopituitarism after Cardiac Surgery

Abstract

Coronary Artery Bypass Grafting (CABG) surgery is identified in case reports as a rare cause of pituitary apoplexy, postulated to be caused by sustained hypotension due to intraoperative extracorporeal circulation. This typically presents with acute neurological manifestations and evidence of pituitary infarction on Magnetic Resonance Imaging (MRI). Here, we present a case of panhypopituitarism without apoplexy weeks after CABG, which presented with nonspecific signs and without definite neuroimaging abnormalities. SM, a 57 year old man with Type 1 Diabetes underwent elective CABG. His initial postoperative course was uneventful. On review at 4 weeks, his sternotomy wound was slow to heal. At 6 weeks, there was wound dehiscence and he was admitted for management of this. He noted a number of significant hypoglycaemic events over the preceding 10 days, despite a 30% reduction in daily insulin over that period. On readmission sodium was reduced at 118mmol/L – normal 6 weeks prior. This was felt to be SIADH secondary to infection, supported by raised urinary sodium and low plasma osmolality. Fluid restriction, however, led to no improvement. He continued to experience hypoglycaemia and erratic glycemic control. Persistent hypotension was then noted, though initially attributed to diuretics. Thyroid function showed low T4 and TSH levels. Panhypopituitarism was confirmed with markedly low Growth Hormone, IGF-1, Prolactin, FSH, LH and 8am cortisol. Adrenal response was absent on short Tetracosactide testing. MRI pituitary was unremarkable. Anterior Pituitary Hormone replacement with Levothyroxine, Hydrocortisone and Somatropin was commenced. Blood pressure improved and electrolytes normalised. 1 year later, SM’s pituitary hormones were maintained within normal ranges with exogenous replacement. However, glycemic control has been challenging, due to loss of counterregulatory hormonal responses to hypoglycaemia. Panhypopituitarism is rarely reported after CABG and mostly involves apoplexy or infarction of a pre-existing pituitary adenoma, with characteristic findings on neuroimaging. These cases relate to alterations in blood flow through the pituitary on ‘bypass’ and highlight the intrinsic vulnerability of the pituitary vasculature. This case is unusual in a number of respects - presentation weeks after surgery with nonspecific findings - poor wound healing and decreased insulin requirements, rather than acute neurological manifestations postoperatively. Previous reports have demonstrated pre-existing pituitary adenomas or evidence of pituitary infarction on MRI. Despite clear biochemical Panhypopituitarism, the MRI here shows a normal gland. Finally, this case reiterates the need for vigilance for subtle and delayed manifestations of pituitary dysfunction post Cardiac Surgery with intervention, prior to life threatening overt glucocorticoid deficiency.